PMID- 31761324
OWN - NLM
STAT- MEDLINE
DCOM- 20200812
LR  - 20200812
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 522
IP  - 2
DP  - 2020 Feb 5
TI  - Chaperone-mediated autophagy regulates apoptosis and the proliferation of colon 
      carcinoma cells.
PG  - 348-354
LID - S0006-291X(19)32207-7 [pii]
LID - 10.1016/j.bbrc.2019.11.081 [doi]
AB  - Chaperone-mediated autophagy (CMA) is one of the three types of autophagy. In 
      recent years, CMA has been shown to be associated with the pathogenesis of 
      several types of cancer. However, whether CMA is involved in the pathogenesis of 
      colorectal cancer (CRC) remains unclear. In this study, we investigated CMA 
      activity in tissue specimens from CRC patients and mouse models of 
      colitis-associated CRC (induced by administration of AOM plus DSS). In addition, 
      we down-regulated CMA in CT26 colon carcinoma cells stably transfected with a 
      vector expressing a siRNA targeting LAMP-2A, the limiting component in the CMA 
      pathway, to explore the role of CMA in these cells. Apoptosis was detected using 
      TUNEL assay, and the apoptosis-related proteins were detected using western 
      blotting. Cell proliferation was assessed using MTT assay, Ki-67 labelling and 
      western blotting for PCNA. We found that LAMP-2A expression was significantly 
      increased in CRC patients and mouse models and varied according to the stage of 
      the disease. Inhibition of CMA in CT26 cells facilitated apoptosis, as evidenced 
      by increased TUNEL immunolabeling, increased expression of Bax and Bnip3, and 
      decreased expression of Bcl-2. Cell proliferation assays showed that inhibition 
      of CMA impeded the proliferation of CT26 cells. These data support the hypothesis 
      that CMA is up-regulated in CRC, and inhibition of CMA may be a new therapeutic 
      strategy for CRC patients.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Peng, Jie-Qiong
AU  - Peng JQ
AD  - School of Medicine and Life Sciences, University of Jinan-Shandong Academy of 
      Medical Sciences, Jinan, China; Department of Oncology, Shandong Cancer Hospital 
      and Institute, Shandong First Medical University and Shandong Academy of Medical 
      Sciences, Jinan, China.
FAU - Han, Shu-Mei
AU  - Han SM
AD  - Department of Oncology, Shandong Cancer Hospital and Institute, Shandong First 
      Medical University and Shandong Academy of Medical Sciences, Jinan, China.
FAU - Chen, Ze-Hao
AU  - Chen ZH
AD  - Shandong First Medical University, Taian, Shandong, China.
FAU - Yang, Jing
AU  - Yang J
AD  - Department of Oncology, Shandong Cancer Hospital and Institute, Shandong First 
      Medical University and Shandong Academy of Medical Sciences, Jinan, China.
FAU - Pei, Yan-Qing
AU  - Pei YQ
AD  - Department of Oncology, Shandong Cancer Hospital and Institute, Shandong First 
      Medical University and Shandong Academy of Medical Sciences, Jinan, China.
FAU - Bao, Cong
AU  - Bao C
AD  - Department of Pathology, Pingyi County People's Hospital, Linyi, Shandong, 
      273300, China.
FAU - Qiao, Lei
AU  - Qiao L
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education, Chinese National Health Commission and Chinese Academy of 
      Medical Sciences, The State and Shandong Province Joint Key Laboratory of 
      Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, 107 
      Wenhuaxi Road, 250012, Jinan, China.
FAU - Chen, Wen-Qiang
AU  - Chen WQ
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education, Chinese National Health Commission and Chinese Academy of 
      Medical Sciences, The State and Shandong Province Joint Key Laboratory of 
      Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, 107 
      Wenhuaxi Road, 250012, Jinan, China. Electronic address: 199262000802@sdu.edu.cn.
FAU - Liu, Bo
AU  - Liu B
AD  - Department of Oncology, Shandong Cancer Hospital and Institute, Shandong First 
      Medical University and Shandong Academy of Medical Sciences, Jinan, China. 
      Electronic address: 15553115688@163.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20191121
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (LAMP2 protein, human)
RN  - 0 (Lysosomal-Associated Membrane Protein 2)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - *Chaperone-Mediated Autophagy
MH  - Colonic Neoplasms/*pathology
MH  - Humans
MH  - Lysosomal-Associated Membrane Protein 2/metabolism
MH  - Male
MH  - Mice, Inbred BALB C
MH  - Neoplasm Staging
OTO - NOTNLM
OT  - Apoptosis
OT  - Chaperone-mediated autophagy
OT  - Colorectal cancer
OT  - Proliferation
EDAT- 2019/11/26 06:00
MHDA- 2020/08/13 06:00
CRDT- 2019/11/26 06:00
PHST- 2019/11/01 00:00 [received]
PHST- 2019/11/13 00:00 [accepted]
PHST- 2019/11/26 06:00 [pubmed]
PHST- 2020/08/13 06:00 [medline]
PHST- 2019/11/26 06:00 [entrez]
AID - S0006-291X(19)32207-7 [pii]
AID - 10.1016/j.bbrc.2019.11.081 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2020 Feb 5;522(2):348-354. doi: 
      10.1016/j.bbrc.2019.11.081. Epub 2019 Nov 21.